Myopia affects approximately 25% of the U.S. population, and as high as 80% of the Asian population in some countries. High degrees of myopia (such as >8 diopters, for example) are less common, but are associated with progressive chorioretinal degeneration. In the subset of high myopes who develop this degeneration (pathologic myopia) irreversible visual loss occurs, often during the fifth and sixth decades of life. In Asia, pathologic myopia is the leading cause of untreatable blindness, affecting approximately 1% of the population. At present, there is no proven effective treatment for pathologic myopia.
In degenerative myopia there is progressive axial enlongation of the eye. The excessive axial enlargement in degenerative myopia causes stretching and thinning of the ocular coats (sclera and chorioretinal tissues). Because this stretching and thinning occurs preferentially in the posterior pole and involves the macula, eyes with degenerative myopia are subject to visual loss. The causes of scleral thinning and stretching in degenerative myopia are incompletely understood, but enhanced turnover of scleral collagen and alteration of scleral glycosaminoglycans are contributory in the disease. As the mechanical properties of the sclera are altered in myopia, the eye is prone to stretching due to the load effect of intraocular pressure. Currently, there are no proven means to prevent the excessive ocular enlargement that occurs in degenerative myopia. Were it possible to retard or prevent ocular enlargement, progression of myopia could be diminished and visual loss prevented at least in part. Increasing the tensile strength or modulus of the sclera is a means to prevent ocular enlargement and reduce progression of myopia.
U.S. Pat. No. 5,756,541 is directed to methods to improve visual acuity including administering a photoactive compound in an amount sufficient to localize to a target ocular tissue and irradiating the target tissue with light from a laser, wherein the wavelength of radiation is absorbed by the photoactive compound and the radiation is conducted for a time and at an intensity sufficient to improve visual acuity. In specific embodiments, the photoactive compound is a green porphyrin. U.S. Pat. No. 5,910,510 is directed to an identical method having a particular irradiation timing.
U.S. Pat. No. 5,798,349 regards methods to treat conditions of the eye characterized by unwanted neovasculature, such as AMD, by administering a liposomal formulation of a green porphyrin in an amount and time sufficient to localize in the neovasculature, followed by irradiation of the neovasculature with laser light, wherein the light absorbed by the green porphyrin occludes the neovasculature. In the related U.S. Pat. No. 6,225,303, the irradiance is in a range from about 300 mW/cm2 to about 900 mW/cm2.
U.S. Pat. No. 6,128,525 is directed to method and apparatus controlling dosimetry of photodynamic therapy.
U.S. Pat. No. 5,935,942 regards methods of occluding vasculature in a mammalian eye including co-administering intravenously a fluorescent dye encapsulated with heat-sensitive liposomes and a tissue-reactive agent activated by irradiation. The liposomes are heated in the eye to release their contents, wherein the tissue-reactive agent remains inactive, followed by monitoring of fluorescent dye flow within the vasculature. The tissue-reactive agent is activated in the vasculature having subnormal blood flow, such that the activated agent chemically occludes the vasculature. The related U.S. Pat. No. 6,140,314 methods further comprise co-administration of a tissue-specific factor effective to impair growth or regeneration of a blood vessel. The related U.S. Pat. No. 6,248,727 regards related diagnostic reagents and kits.